Chemical Injuries — MCQs
Following injury to the right temple region, a patient complains of pain in the right eye and loss of vision. On examination, the eye movements are normal, and the pupil normally reacts to light. The affected eye shows increased intraocular pressure of 32 mmHg (normal: 10-21 mmHg), mild corneal edema, and a small hyphema visible in the anterior chamber. The diagnosis is
All of the following are complications of traumatic hyphema except which of the following?
Vitreous humor is preserved in suspected poisoning with:
Ischemic necrosis in alkali burn corresponds to which stage?
What is the key pathophysiological difference between acid and alkali injuries in terms of tissue necrosis?
A 25-year-old person developed right corneal opacity following injury to the eye. Keratoplasty of right eye was done and vision was restored. Medico-legally such injury is:
Most serious injury to the eye is caused by:
Gastric lavage is contraindicated in?
What does the following image show?
True about acid injury to eye are all except?
Chemical Injuries Indian Medical PG Practice Questions and MCQs
Question 1: Following injury to the right temple region, a patient complains of pain in the right eye and loss of vision. On examination, the eye movements are normal, and the pupil normally reacts to light. The affected eye shows increased intraocular pressure of 32 mmHg (normal: 10-21 mmHg), mild corneal edema, and a small hyphema visible in the anterior chamber. The diagnosis is
- A. Traumatic glaucoma (Correct Answer)
- B. Optic nerve atrophy
- C. Sub-arachnoid haemorrhage
- D. Functional loss of vision
Explanation: ***Traumatic glaucoma*** - Increased **intraocular pressure (32 mmHg)** after a **temple injury** with **corneal edema** and **hyphema** are classic signs of traumatic glaucoma. - The hyphema (blood in the anterior chamber) obstructs the **trabecular meshwork**, impeding aqueous humor outflow and leading to elevated IOP. *Optic nerve atrophy* - While optic nerve atrophy can cause **vision loss**, it is a chronic condition and typically not an acute presentation following trauma unless there is direct optic nerve damage. - It would not explain the acute findings of **hyphema**, **corneal edema**, or acutely elevated **intraocular pressure**. *Sub-arachnoid haemorrhage* - A **sub-arachnoid hemorrhage** might present with headache and loss of consciousness, or **papilledema** in severe cases, but typically would not cause such specific eye findings as **hyphema** or **corneal edema** from elevated IOP. - While a blow to the head could cause this, the direct eye findings point to a local ocular issue. *Functional loss of vision* - **Functional vision loss** (or psychogenic vision loss) is a diagnosis of exclusion where no organic cause can be found. - The presence of clear organic signs such as **hyphema**, **corneal edema**, and significantly elevated **intraocular pressure** rules out a functional cause.
Question 2: All of the following are complications of traumatic hyphema except which of the following?
- A. Pupillary Block
- B. Posterior synechiae
- C. Rebleeding
- D. Corneal Ulcer (Correct Answer)
Explanation: ***Corneal Ulcer*** - A **corneal ulcer** is typically caused by infection, trauma, or exposure keratitis and is not a direct complication of blood in the anterior chamber from a **traumatic hyphema**. - While prolonged elevation of **intraocular pressure** from hyphema could theoretically impair corneal health, a direct ulcer is not a typical or primary complication. *Rebleeding* - **Rebleeding** is a common and serious complication of hyphema, usually occurring 2-7 days after the initial injury. - It often results in a more significant bleed and carries a higher risk of complications such as **elevated intraocular pressure** and **blood staining of the cornea**. *Pupillary Block* - **Pupillary block** can occur if the amount of blood from the hyphema prevents the flow of aqueous humor from the posterior to the anterior chamber. - This blockage leads to a buildup of **aqueous humor** in the posterior chamber, causing the iris to bow forward and potentially precipitating **acute angle-closure glaucoma**. *Posterior synechiae* - **Posterior synechiae** can develop due to inflammation (uveitis) associated with the hyphema, where the iris adheres to the anterior lens capsule. - This complication can lead to **irregular pupil shape**, **pupillary block glaucoma**, or other visual disturbances.
Question 3: Vitreous humor is preserved in suspected poisoning with:
- A. Cyanide
- B. Morphine
- C. Alcohol (Correct Answer)
- D. Carbon monoxide
Explanation: ***Alcohol*** - **Vitreous humor** is an ideal sample for postmortem alcohol analysis due to its **sequestration** from other body fluids, which minimizes postmortem production or degradation of alcohol. - Its **avascular nature** and **slow diffusion** rates ensure that the alcohol concentration in the vitreous humor closely reflects the ante-mortem blood alcohol concentration. *Cyanide* - Sampling **vitreous humor** is generally not the primary choice for detecting cyanide because cyanide is rapidly absorbed and metabolized, making its detection more reliable in other tissues. - Cyanide can degrade in biological samples, and its concentration in the vitreous humor may not accurately reflect the lethal dose or recent exposure. *Morphine* - While **vitreous humor** can be used for opiate detection, **blood and urine** are generally preferred for initial screening and quantitative analysis of morphine. - Morphine undergoes metabolism during its elimination, and its distribution into the vitreous humor might not always accurately reflect the **pharmacodynamics** or precise time of exposure compared to blood. *Carbon monoxide* - **Carbon monoxide (CO) poisoning** is primarily diagnosed by measuring **carboxyhemoglobin levels** in blood, as CO binds avidly to hemoglobin. - The vitreous humor is not a suitable sample for detecting carbon monoxide or carboxyhemoglobin as it lacks red blood cells and hemoglobin, which are the targets of CO toxicity.
Question 4: Ischemic necrosis in alkali burn corresponds to which stage?
- A. Stage II (Correct Answer)
- B. Stage I
- C. Stage III
- D. Stage IV
Explanation: ***Stage II*** - **Ischemic necrosis** in an alkali burn corresponds to Stage II, indicating a more severe and damaging effect on the tissue. - This stage involves significant cell death due to **loss of blood supply**, often seen in deeper tissue penetration by the corrosive agent [1]. *Stage I* - Stage I describes **edema** and **epithelial erosion** without significant tissue necrosis or ischemia [1]. - This stage is typically characterized by superficial damage, good perfusion, and a relatively rapid recovery without permanent scarring. *Stage III* - Stage III represents a severely advanced burn that progresses beyond necrosis to **perforation** of the esophagus or other affected organs. - At this stage, the tissue damage is extensive, leading to a high risk of complications like **mediastinitis** or **peritonitis**. *Stage IV* - While not a universally recognized stage for alkali burns, if used, Stage IV would imply **incurable damage** or **systemic complications** that threaten the patient's life, possibly involving multiple organ failure due to sepsis or other severe sequelae. - This stage would signify irreversible harm beyond localized tissue destruction, often leading to a fatal outcome. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 53-56, 61-62.
Question 5: What is the key pathophysiological difference between acid and alkali injuries in terms of tissue necrosis?
- A. Acid injuries cause coagulative necrosis
- B. Alkali injuries lead to deeper tissue damage
- C. Acid injuries are less severe than alkali injuries
- D. Alkali injuries cause liquefactive necrosis (Correct Answer)
Explanation: ***Alkali injuries cause liquefactive necrosis*** - **Alkali burns** result in **liquefaction necrosis**, which involves the dissolution of tissue and cells, leading to a much deeper and progressive injury as the alkali penetrates further into tissues. - This is the **key pathophysiological difference** that distinguishes alkali from acid injuries - the TYPE of necrosis (liquefactive vs coagulative). - This type of necrosis allows the alkali to continue damaging underlying tissues and can lead to more extensive and severe scarring and complications. *Acid injuries cause coagulative necrosis* - While this statement is **medically true**, it only describes what acids do without explicitly stating the **difference** or comparison with alkali injuries. - The question asks for the KEY **difference**, and this option presents only one half of the comparison. - **Acid burns** typically cause **coagulation necrosis**, forming a coagulum or eschar that precipitates proteins and creates a barrier, thereby limiting the depth of penetration. - The correct answer (alkali → liquefactive necrosis) better captures the distinguishing pathophysiological feature. *Alkali injuries lead to deeper tissue damage* - This statement is true but serves as a **consequence** of the underlying **liquefactive necrosis** rather than the primary pathophysiological mechanism itself. - The liquefaction process continuously destroys cells and extracellular matrix, enabling the caustic agent to propagate deeply into the tissue. - This describes the OUTCOME rather than the KEY pathophysiological mechanism. *Acid injuries are less severe than alkali injuries* - This is a **generalization about severity** rather than identifying the specific pathophysiological mechanism of tissue death. - While generally true due to the **coagulation necrosis** limiting the depth of penetration of acids, severity can vary based on concentration, duration of exposure, and other factors. - The formation of a protective eschar in acid burns often prevents further significant tissue destruction, unlike the progressive damage seen in alkali burns.
Question 6: A 25-year-old person developed right corneal opacity following injury to the eye. Keratoplasty of right eye was done and vision was restored. Medico-legally such injury is:
- A. Dangerous
- B. Grievous
- C. Simple (Correct Answer)
- D. Non-grievous
Explanation: ***Simple*** - The injury resulted in corneal opacity that was **successfully treated with keratoplasty and vision was restored**. - Under IPC Section 320, **grievous hurt** requires **permanent privation of sight**, not temporary visual impairment. - Since vision was restored after treatment, there is **no permanent damage**, making this a **simple injury**. - Simple injuries may require medical treatment and cause temporary incapacitation, but do not result in permanent impairment. *Grievous* - Grievous hurt under IPC Section 320 includes **permanent privation of the sight of either eye**. - The key word is **permanent** - since vision was restored after keratoplasty, the visual loss was temporary, not permanent. - This injury does not meet the criteria for grievous hurt despite requiring surgical intervention. *Dangerous* - "Dangerous" is not a specific medico-legal classification of injury under IPC Section 320. - This term may describe the potential severity but is not used to categorize injuries legally. *Non-grievous* - While technically correct (as non-grievous means not grievous), the proper legal term is **"simple injury"**. - In medico-legal practice, injuries are classified as either grievous or simple, not as "non-grievous".
Question 7: Most serious injury to the eye is caused by:
- A. Nitric acid
- B. Hydrochloric acid
- C. Lime (Correct Answer)
- D. Sulphuric acid
Explanation: ***Lime*** - **Lime (calcium hydroxide)** is an **alkali** that causes **liquefactive necrosis** of ocular tissues, leading to deep penetration and severe, progressive damage. - Alkaline burns saponify cell membranes, resulting in continuous tissue destruction and potentially **corneal opacification**, **limbal ischemia**, and **perforation**. *Nitric acid* - **Nitric acid** is a strong acid that causes **coagulation necrosis**, which tends to create a protective barrier on the tissue. - While serious, this barrier often limits deeper penetration and tissue destruction compared to alkalis. *Hydrochloric acid* - **Hydrochloric acid** is also a strong acid and causes **coagulation necrosis**, similar to nitric acid. - This type of injury typically results in superficial damage to the eye, as the denatured proteins form a physical barrier. *Sulphuric acid* - **Sulphuric acid**, another strong acid, also primarily causes **coagulation necrosis**. - Although it can dehydrate tissues and cause significant superficial damage, its effect is generally less severe and penetrating than strong alkalis.
Question 8: Gastric lavage is contraindicated in?
- A. Bicarbonate
- B. Hydrocarbons (Correct Answer)
- C. Organo-Phosphosphate poisoning
- D. PCM toxicity
Explanation: ***Hydrocarbons*** - Gastric lavage is contraindicated in **hydrocarbon poisoning** due to the high risk of **aspiration** [2]. - Aspiration of hydrocarbons can lead to severe **chemical pneumonitis**, which is often more life-threatening than the systemic toxicity from ingestion [2]. *Bicarbonate* - Ingesting a large amount of bicarbonate can cause **alkalosis** and electrolyte imbalances. - While gastric lavage is not typically the primary treatment for mild bicarbonate overdose, it is not absolutely contraindicated in cases of massive ingestion where there is a clear benefit to removing unabsorbed substance, especially if performed with proper airway protection [1], [3]. *Organo-Phosphosphate poisoning* - Gastric lavage is generally recommended for **organophosphate poisoning** if the patient presents within 1-2 hours of ingestion and is awake with an intact gag reflex, or with a protected airway [2]. - This helps remove unabsorbed poison and can reduce the systemic absorption of these highly toxic compounds. *PCM toxicity* - For **paracetamol (PCM) toxicity**, gastric lavage can be considered if the patient presents within 1-2 hours of ingestion and has ingested a potentially toxic dose, especially when activated charcoal is not immediately available or contraindicated [4]. - The primary treatment for PCM toxicity involves **N-acetylcysteine (NAC)**, but gastric emptying can play a role in reducing initial absorption [4].
Question 9: What does the following image show?
- A. Anterior uveitis
- B. Membranous conjunctivitis
- C. Pannus (Correct Answer)
- D. Pseudomembranous conjunctivitis
Explanation: ***Pannus*** - The image distinctly shows **new blood vessels growing into the cornea** from the limbus, which is characteristic of pannus formation. This vascularization often accompanies chronic inflammation or hypoxia. - This condition is a hallmark of certain ophthalmic diseases, such as **trachoma** or chronic irritation from prolonged **contact lens wear**. *Anterior uveitis* - Anterior uveitis presents with inflammation of the iris and ciliary body, typically causing **ciliary flush**, **miosis**, and cells/flare in the anterior chamber, which are not the primary features shown. - While uveitis can sometimes lead to corneal changes, the prominent **vascularization extending onto the cornea** is not its defining visual characteristic. *Membranous conjunctivitis* - Membranous conjunctivitis is characterized by the formation of a **true membrane on the conjunctiva** that binds tightly to the underlying epithelium, often caused by severe bacterial infections like *Corynebacterium diphtheriae*. - The image does not show a membrane on the conjunctival surface; instead, it highlights **corneal vascularization**. *Pseudomembranous conjunctivitis* - Pseudomembranous conjunctivitis involves a **fibrinous exudate loosely adherent** to the conjunctiva, which can be peeled off without significant bleeding, as seen in adenoviral conjunctivitis. - The findings in the image, specifically **vascular ingrowth into the cornea**, are not consistent with the appearance of a pseudomembrane on the conjunctiva.
Question 10: True about acid injury to eye are all except?
- A. more destructive than alkali injuries (Correct Answer)
- B. steroids are used to control inflammation
- C. makes a barrier and prevent deeper penetration
- D. glaucoma is most preventable complication following acid injury
Explanation: ***more destructive than alkali injuries*** - This statement is **false**. **Alkali burns** are generally more severe than acid burns because alkalis have **liquefactive necrosis**, which allows them to penetrate deeper into ocular tissues. - Acids cause **coagulative necrosis**, which forms a protective barrier that limits further penetration, making them typically less destructive than alkali injuries. *steroids are used to control inflammation* - **Topical corticosteroids** are commonly used in the management of ocular chemical burns, including acid injuries, to help **control inflammation** and reduce the risk of secondary complications. - However, their use must be carefully monitored due to potential side effects like increased intraocular pressure and delayed corneal healing. *makes a barrier and prevent deeper penetration* - **Acidic substances** cause **coagulative necrosis** of the superficial tissues, which creates a protective barrier of denatured proteins. - This barrier helps to prevent the acid from penetrating deeper into the ocular structures, thus often limiting the extent of damage compared to alkali burns. *glaucoma is most preventable complication following acid injury* - **Glaucoma** is indeed a significant complication of ocular acid injuries and can be prevented through **immediate copious irrigation**, control of inflammation, and monitoring of intraocular pressure. - While various complications can occur (corneal opacification, symblepharon, limbal stem cell deficiency), glaucoma prevention through early intervention and appropriate medical management is a key focus in acute management, making this statement acceptable as true.
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